IBS Is Linked to Bowel Defects

AUGUST 01, 2004

Serotonin plays a critical role in the regulation of gastrointestinal
(GI) motility, secretion, and sensation. Irritable bowel syndrome
(IBS) is associated with clinical symptoms that include alterations in
normal patterns of motility, secretion, and sensation. The role of
serotonin in the pathophysiology of IBS, however, remains unclear.

In the June 2004 issue of Gastroenterology, researchers
reported the results of a study aimed at testing whether enteric
serotonin signaling is defective in patients with IBS and in patients
with ulcerative colitis (UC). Key elements of serotonin signaling,
including measures of serotonin content, release, and reuptake,
were analyzed in rectal biopsy samples from patients with UC
(n = 22), patients with IBS with diarrhea (IBS-D; n = 15), patients
with IBS with constipation (IBS-C; n = 16), and controls (n = 34).

Results showed that mucosal serotonin, tryptophan hydroxylase
1 messenger RNA (mRNA), serotonin transporter mRNA,
and serotonin transporter immunoreactivity were all significantly
reduced in patients with UC, IBS-D, and IBS-C. The enterochromaffin
cell population was reduced in samples from patients with
severe UC but was unchanged in samples from patients with
IBS. No changes were detected in any of the disease samples
relative to the control samples when serotonin release was
investigated under basal and mechanical stimulation conditions.
The authors concluded that both UC and IBS are associated with
molecular changes in serotonergic signaling mechanisms and
that these data support the assertion that disordered GI function
in IBS involves changes intrinsic to the bowel.